Ask about this productRelated genes to: GPR87 Blocking Peptide
- Gene:
- GPR87 NIH gene
- Name:
- G protein-coupled receptor 87
- Previous symbol:
- GPR95
- Synonyms:
- -
- Chromosome:
- 3q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-23
- Date modifiied:
- 2016-10-06
Related products to: GPR87 Blocking Peptide
Related articles to: GPR87 Blocking Peptide
- Prior to 2024, pulmonary hypertension (PH) associated with chronic lung diseases (group 3 in the classification of PH) was subclassified according to the type of ventilatory disorder (obstructive, restrictive lung disease or mixed patterns) and not according to the lung disease itself. In 2024, the 7th World Symposium on PH proposed a revised classification, describing associations with specific lung diseases, such as COPD, interstitial lung disease and combined pulmonary fibrosis and emphysema. This update highlights the distinct pathophysiological mechanisms, clinical manifestations, outcomes and management strategies across these subgroups. Of note, a nonparenchymal restrictive lung disease subgroup has been identified, which includes patients with hypoventilation syndromes (due to kyphoscoliosis, diaphragmatic diseases, obesity hypoventilation syndrome, central hypoventilation syndromes, ) or pneumonectomy. Paradoxically, despite being one of the earliest forms of PH described, PH associated with nonparenchymal restrictive lung diseases remains among the least studied subtypes. As with all causes of group 3 PH, the primary focus of management is to address the underlying condition whenever possible. There are few data on the efficacy, safety and tolerability of the treatments approved for pulmonary arterial hypertension in this specific population. This review aims to provide updates on this condition and its management, to highlight the mechanisms of PH in each nonparenchymal restrictive lung disease and to study the relevance of the new classification and the necessary avenues of research. - Source: PubMed
Publication date: 2026/03/11
Jutant Etienne-MarieHumbert MarcMontani DavidKhoury JohadAdir Yochai - : Patients with "driver gene-negative" LUAD lack effective targeted therapies. This study aimed to elucidate the role of the glycolysis pathway in driver gene-negative LUAD to identify key genes and potential therapeutic targets. : Bulk RNA sequencing data from 49 patients with driver gene-negative LUAD were analyzed. The driver gene-negative status of patients was confirmed by immunoblotting. Gene set enrichment analysis (GSEA) was conducted on six hallmark pathways related to glycolysis. Additionally, key genes were identified and a risk score model was constructed. Finally, single-cell RNA sequencing data were processed using the Seurat package for data cleaning, dimensionality reduction clustering, and cell type identification. : GSEA analysis revealed significant enrichment of the glycolysis pathway in driver gene-negative LUAD. Differential expression analysis identified 144 genes associated with the glycolysis pathway. Six glycolysis-related genes (ANKZF1, GPR87, KIF2A, LCT, MIF, SDHC) were identified associated with poor prognosis. Single-cell sequencing analysis validated the key role of MIF in the glycolysis process and revealed a positive feedback regulatory axis between MIF and HIF-1α, which may promoting glycolysis and malignant transformation. : This study elucidated glucose metabolic reprogramming mechanisms and highlighted the MIF-HIF-1α axis as a promising therapeutic target in "driver gene-negative" LUAD, which may offer new avenues for improving outcomes, particularly those lacking conventional targeted therapy options. - Source: PubMed
Publication date: 2025/10/10
Yang Hao-ShuaiLi Yuan-HaoChen QiLuo Hong-HeYu Qi-DuoHan YuZhu WeijieZhang JinLiang Chao-Yang - Histones are the fundamental building blocks of chromatin and serve as pivotal regulators of gene expression. Differential expression and mutations of H3.1 and H3.3 genes have been implicated in the pathogenesis of various cancer types. Mutations in H3.3, especially lysine to methionine substitutions (K27M/K36M), are particularly prevalent. Moreover, genetic alterations such as G34R/W/V/L, as well as variations in and genes, have also been identified. Despite high similarity in amino acid sequences, H3.1 and H3.3 have discrete functions in cancer. In this review, we delve into the recent advances in elucidating the implications of canonical histone H3.1 and its variant H3.3 on chromatin structure and function. Additionally, we explore how potential enhancing factors such as PTEN, MLL5, GPR87 and histone chaperones influence H3.1/H3.3 function. - Source: PubMed
Publication date: 2025/09/24
Wu PengWang LiWen TingChen Qiao Yi - Orphan class A G protein-coupled receptors (GPCRs) are a large and diverse family with broad tissue expression, and their roles in tumors are increasingly recognized. However, their involvement in gastric cancer (GC) remains unclear. We performed survival and differential expression analyses to characterize orphan class A GPCR expression patterns in stomach adenocarcinoma (STAD). A prognostic risk model was developed using univariate Cox and LASSO regression analysis and validated in the GEO database. Drug sensitivity and immune infiltration were evaluated across different risk groups. The role of GPR176 in GC and its relationship with tumor immunity were further explored using cellular assays. A model incorporating nine orphan class A GPCRs (GPR15, GPR150, GPR176, GPR4, GPR26, GPR78, GPR101, GPR34, and GPR87) was constructed, showing a positive correlation with M2 macrophages and naive B cells. Low-risk patients showed higher sensitivity to AZD6482, BX.795, GDC0941, and pazopanib. GPR176 was found to be upregulated in GC, and functional assays demonstrated that its knockdown suppressed proliferation and migration in the GC cell lines SGC-7901 and HGC-27. GPR176 also modulated the Wnt/β-catenin pathway and M2 macrophage polarization. These findings may provide new insights into the role of orphan class A GPR genes in STAD and identify GPR176 as a new therapeutic target for GC. - Source: PubMed
Publication date: 2025/07/11
Lin JiahuiKe LinglingCheng ShaLu WeiHu YananHe XiyiLuo TingtingLiu YutingXu CanxiaQi Jian - GPR87 is an orphan G-protein-coupled receptor (GPCR) that represents a potential molecular target for developing novel drugs aimed at treating squamous cell carcinomas (SCCs) or adenocarcinomas of the lungs and bladder. - Source: PubMed
Rani MuktaSharma Amit KumarNischal AnuradhaKhattri SanjaySahoo Ganesh ChandraSingh Rajesh K